PMID- 15720439
OWN - NLM
STAT- MEDLINE
DCOM- 20050412
LR  - 20181113
IS  - 0019-2805 (Print)
IS  - 1365-2567 (Electronic)
IS  - 0019-2805 (Linking)
VI  - 114
IP  - 3
DP  - 2005 Mar
TI  - Migration of polymorphonuclear leucocytes is influenced by dendritic cells.
PG  - 375-85
AB  - Dendritic cells (DCs) are the most potent antigen-presenting cells and populate 
      many tissues where they may participate in inflammatory reactions. The 
      infiltration of polymorphonuclear leucocytes (PMNLs) into tissues is a prominent 
      feature of inflammation. The mechanisms of PMNL recruitment depend on chemotactic 
      factors and adhesion molecules expressed on endothelial cells. The aim of the 
      present study was to determine whether DCs participate in the early recruitment 
      of PMNLs. Dendritic cells derived from peripheral blood monocytes were used for 
      this study. PMNLs incubated with culture supernatant (CS) from untreated or from 
      tumour necrosis factor-alpha (TNF-alpha)-treated (1 hr, 100 U/ml, 37 degrees ) 
      monocyte-derived DCs (moDCs) had increased surface expression of both CD11b and 
      CD18. Moreover, both untreated and TNF-alpha-treated moDCs induced PMNL 
      chemotaxis. By blocking CXCL8, CXCL5, CXCL7 and Pan GRO (CXCL1, CXCL2, CXCL3), we 
      observed that CXCL8/interleukin-8 might be the chemokine that induced the PMNL 
      chemotactic activity in the CS of untreated and TNF-alpha-treated moDC. 
      Furthermore, we investigated the regulation of CXCL8 production in moDCs by 
      adhesion molecule engagement. Our data demonstrated that CD31, CD18, CD29 and 
      CD49d participated in the adhesion of immature moDCs to endothelium. Moreover, 
      engagement of domains 1-3 of CD31, but not of CD29 or CD18, decreased the 
      production of CXCL8 by immature but not mature moDCs (which display lower CD31 
      levels than immature moDCs). Overall, these results suggest that DCs not only 
      trigger a specific immune response, but also the innate immune response by 
      recruiting PMNLs. Furthermore, our results also suggest that CXCL8 production by 
      immature DCs might be regulated by signalling through CD31 during their migration 
      through the vascular endothelium.
FAU - Scimone, M Lucila
AU  - Scimone ML
AD  - Laboratorio de Inmunogenetica, Hospital de Clinicas Jose de San Martin, 
      Departamento de Microbiologia, Parasitologia e Inmunologia, Facultad de Medicina, 
      Universidad de Buenos Aires, Buenos Aires, Argentina.
FAU - Lutzky, Viviana P
AU  - Lutzky VP
FAU - Zittermann, Sandra I
AU  - Zittermann SI
FAU - Maffia, Paulo
AU  - Maffia P
FAU - Jancic, Carolina
AU  - Jancic C
FAU - Buzzola, Fernanda
AU  - Buzzola F
FAU - Issekutz, Andrew C
AU  - Issekutz AC
FAU - Chuluyan, H Eduardo
AU  - Chuluyan HE
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Immunology
JT  - Immunology
JID - 0374672
RN  - 0 (CD11b Antigen)
RN  - 0 (CD18 Antigens)
RN  - 0 (CXCL3 protein, human)
RN  - 0 (Chemokines, CXC)
RN  - 0 (Culture Media, Conditioned)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (Interleukin-8)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 207137-56-2 (Interleukin-4)
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
SB  - IM
MH  - Animals
MH  - Bone Marrow/immunology
MH  - CD11b Antigen/metabolism
MH  - CD18 Antigens/metabolism
MH  - Cell Adhesion/immunology
MH  - Cells, Cultured
MH  - Chemokines, CXC
MH  - Chemotaxis, Leukocyte/*immunology
MH  - Culture Media, Conditioned
MH  - Dendritic Cells/*immunology
MH  - Endothelium, Vascular/immunology
MH  - Granulocyte-Macrophage Colony-Stimulating Factor/immunology
MH  - Humans
MH  - Inflammation/*immunology
MH  - Intercellular Signaling Peptides and Proteins
MH  - Interleukin-4/immunology
MH  - Interleukin-8/biosynthesis/immunology
MH  - Lymphocyte Activation/immunology
MH  - Male
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Neutrophils/*immunology
MH  - Tumor Necrosis Factor-alpha/immunology
PMC - PMC1782099
EDAT- 2005/02/22 09:00
MHDA- 2005/04/13 09:00
PMCR- 2006/03/01
CRDT- 2005/02/22 09:00
PHST- 2005/02/22 09:00 [pubmed]
PHST- 2005/04/13 09:00 [medline]
PHST- 2005/02/22 09:00 [entrez]
PHST- 2006/03/01 00:00 [pmc-release]
AID - IMM2104 [pii]
AID - 10.1111/j.1365-2567.2005.02104.x [doi]
PST - ppublish
SO  - Immunology. 2005 Mar;114(3):375-85. doi: 10.1111/j.1365-2567.2005.02104.x.